Role of oxygen in the production of human decompression sickness

1987 ◽  
Vol 63 (6) ◽  
pp. 2380-2387 ◽  
Author(s):  
P. K. Weathersby ◽  
B. L. Hart ◽  
E. T. Flynn ◽  
W. F. Walker

In the calculation of decompression schedules, it is commonly assumed that only the inert gas needs to be considered; all inspired O2 is ignored. Animal experiments have shown that high O2 can increase risk of serious decompression sickness (DCS). A trial was performed to assess the relative risks of O2 and N2 in human no-decompression dives. Controlled dives (477) of 30- to 240-min duration were performed with subjects breathing mixtures with low (0.21–0.38 ATA) or high (1.0–1.5 ATA) Po2. Depths were chosen by a sequential dose-response format. Only 11 cases of DCS and 18 cases of marginal symptoms were recorded despite exceeding the presently accepted no-decompression limits by greater than 20%. Analysis by maximum likelihood showed a shallow dose-response curve for increasing depth. O2 was estimated to have zero influence on DCS risk, although data variability still allows a slight chance that O2 could be 40% as effective as N2 in producing a risk of DCS. Consideration of only inert gases is thus justified in calculating human decompression tables.

1980 ◽  
Vol 190 (2) ◽  
pp. 333-339 ◽  
Author(s):  
M C W Minchin

1. Protoveratrine A increased the release of gamma-amino[3H]butyrate from small slices of rat cerebral cortex. This effect increased with increasing protoveratrine concentration, reaching a maximum at 100 microM. 2. Removal of Ca2+ from the superfusing medium did not change the increase in release due to 10 microM-protoveratrine; however, the Ca2+ antagonists, compound D-600, La3+, Mn2+, Mg2+ and also high Ca2+ concentration inhibited the effect of the alkaloid, as did procaine. 3. Protoveratrine A increased the uptake of 22Na+ into the slices with a similar dose-response curve to that found for gamma-aminobutyrate release. For the most part, the substances that inhibited protoveratrine-stimulated gamma-aminobutyrate release also inhibited 22Na+ uptake, although the correlation was not perfect. 4. Although extracellular Ca2+ is not required for protoveratrine-induced gamma-aminobutyrate release, an increase in Na+ influx that is susceptible to inhibition by some Ca2+ antagonists does appear to be associated with this phenomenon. However, the possibility remains that changes in the free intracellular Ca2+ concentration may be important for transmitter release induced by depolarizing veratrum alkaloids.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 698-698
Author(s):  
John Quilley ◽  
Yue Qiu

P30 Endothelium-dependent vasorelaxant responses to acetylcholine (Ach) in rat aorta are mediated solely by NO. Rings precontracted with U46619 were used to investigate the role of endothelial K + channels. Thus, any effect of K + channel inhibitors on Ach responses in the absence of an effect on those to nitroprusside (NP) can be attributed to interference with Ach-induced stimulation of NO. Vasorelaxant responses to Ach (log EC 50 -7.29M) were abolished by removal of the endothelium or inhibition of NO synthesis with nitroarginine (100μM) which potentiated responses to NP (log EC 50 -9.41M vs -8.47M for control). In the presence of TEA (10mM) to inhibit K + channels, the dose-response curve for Ach, but not NP, was shifted to the right (log EC 50 -6.06). Elevation of extracellular K + (25mM KCl)also shifted the dose-response curve for Ach to the right. Inhibitors of specific types of K + channels: BaCl 2 (30μM), apamin (100nM), glibenclamide (10μM), charybdotoxin (50nM) and iberiotoxin (100nM) were without effect on dose-response curves to either Ach or NP. However, the combination of apamin (100nM) and charybdotoxin (50nM) but not apamin plus iberiotoxin, reduced relaxant responses to Ach (log EC 50 -6.95M) without affecting those to NP.These results confirm that Ach-induced relaxation of rat aorta is mediated entirely by endothelium-derived NO, the release of which apparently involves hyperpolarization of the endothelium. This effect is dependent on activation of a K + channel that is blocked by a combination of apamin/charybdotoxin but neither agent alone, possibly indicating characteristics of both Ca 2+ - activated and voltage-dependent K + channels.


1985 ◽  
Vol 63 (10) ◽  
pp. 1297-1301 ◽  
Author(s):  
C. L. Girard ◽  
J. R. Seoane ◽  
J. J. Matte

Fourteen sheep were used to study the role of gamma-aminobutyric acid (GABA) on the hypothalamic control of feed intake. Injections (1 μL) of pentobarbital (262 nmol) into preoptic and paraventricular areas induced feeding in satiated sheep. Injections of GABA into the same loci gave variable results, probably because the neuronal and glial uptake of GABA limits its effects. Muscimol, a GABA agonist with a higher affinity for postsynaptic GABA receptors than GABA, injected at doses from 0 to 0.750 nmol, gave a cubic dose–response curve; the highest feed intake was measured at 0.5 nmol. The response induced by muscimol was blocked by preinjections of two GABA antagonists, picrotoxin and bicuculline, with picrotoxin being more effective than bicuculline. Muscimol responsive loci were identified mainly in the preoptic, paraventricular, and anterior hypothalamus. The data suggests that neurons sensitive to gamma-aminobutyric acid may be implicated in the control of feed intake in sheep.


1994 ◽  
Vol 266 (3) ◽  
pp. L232-L237
Author(s):  
K. S. Lindeman ◽  
L. B. Fernandes ◽  
T. L. Croxton ◽  
C. A. Hirshman

To elucidate the mechanism of hypoxic relaxation of airway smooth muscle in vitro, we investigated the role of adenosine triphosphate-sensitive potassium (KATP) channels in this response. Second- and third-order porcine bronchial rings were suspended in 10-ml organ baths containing Krebs-Henseleit solution. To demonstrate the presence of KATP channels in this tissue, bronchial rings were contracted with carbachol (1 microM) in the presence of glibenclamide (100 microM), a KATP channel blocker, or the vehicle dimethyl sulfoxide (DMSO) (0.1 ml), and dose-response curves to levcromakalim (a KATP channel opener) or isoproterenol were constructed. In separate experiments, either glibenclamide or DMSO was added to the chamber and rings were contracted with carbachol (1 microM) in the presence of 95% O2-5% CO2. At the plateau, airways were relaxed with either isoproterenol (0.1 or 0.3 microM) or hypoxia (50, 28, or 0% O2, with constant 5% CO2). Glibenclamide, when compared with DMSO, shifted the dose-response curve to levcromakalim, but not to isoproterenol. Glibenclamide attenuated hypoxic relaxation in rings exposed to 50% O2 (from 35 +/- 4% to 23 +/- 3%, n = 6, P < 0.001) and increased the time to 63% relaxation in rings exposed to 50% O2 or to 28% O2. Responses in rings exposed to 0% O2 or to isoproterenol (0.1 or 0.3 microM) were not significantly altered. The ability of glibenclamide to attenuate the maximum response to 50% O2 and to increase the time to 63% relaxation during exposure to 50 or 28% O2 suggests that one component of hypoxic bronchodilation during moderate degrees of hypoxia is opening of KATP channels.


2007 ◽  
Vol 292 (5) ◽  
pp. C1787-C1798 ◽  
Author(s):  
Jing Lu ◽  
Walter F. Boron

Others have shown that H2DIDS reversibly and covalently binds to the first lysine (K) in the SKLIK motif at the extracellular end of transmembrane segment 5 of the Cl-HCO3 exchanger AE1. Here we mutated K558, K559, and/or K562 in the homologous KKMIK motif of human NBCe1-A. We expressed constructs in Xenopus oocytes, and used a two-electrode voltage clamp to test the sensitivity of the NBC current (−160 to +20 mV) to DIDS. A 30-s DIDS exposure decreased the current at 0 mV, and a subsequent albumin wash returned the current to the initial value (less any irreversible DIDS inhibition), permitting the determination of a complete dose-response curve on a single oocyte. For all constructs, the reversible DIDS inhibition of the NBC current decreased at more negative voltages. The apparent inhibitory constant for reversible DIDS binding increased in the sequence RRMIR < KKMIK ( wt, ∼40 μM) < NKMIK ≅ NKMIN ≅ KKMIN < KNMIN ≅ KNMIK < NNMIK < NNMIN (∼400 μM) < DDMID < EEMIE (∼800 μM). Thus the second K is the most important for reversible DIDS blockade. Nevertheless, these mutations had relatively little effect on slope conductance in the absence of DIDS. For KKMIK, RRMIR, NKMIK, KKMIN, KNMIK, and NNMIN, the rates of irreversible inhibition by DIDS roughly parallel the apparent affinities for reversible DIDS binding. The rate was extremely low for DDMID. The fitted maximal inhibitions were 80–91% for the first five constructs, and 66% for NNMIN. Thus DIDS probably reversibly binds before irreversibly reacting with NBCe1-A. Finally, tenidap blocks not only KKMIK, but also NNMIN and EEMIE.


1985 ◽  
Vol 249 (4) ◽  
pp. H851-H858
Author(s):  
H. W. Overbeck

We assessed the role of putative circulating ouabainlike factors on in vivo arteriolar function in rats with very early (less than or equal to 7 days, mean 3 days), benign, one-kidney, one-clip (1K1C) hypertension. Thus we measured vascular responses in vasodilated (nitroprusside or adenosine), vascularly isolated, innervated hindlimb vascular beds of chloralose-anesthetized 1K1C rats perfused with their own blood at 1 ml/min. Complete dose-response curves to norepinephrine in 19 1K1C compared with 25 uninephrectomized (1K) normotensive control rats showed unchanged thresholds and 50% effective dosages. Magnitude of ouabain-induced leftward shifts of the dose-response curve in 29 1K1C and 30 1K rats were similar. In 1K1C, compared with 1K, limb resting resistance was elevated by 45% (P less than 0.001), and limb resistance at maximal vasodilation was elevated by 15% (P less than 0.02). These results provide no evidence in this form and stage of hypertension that humoral ouabainlike inhibitors of the sodium-potassium pump evoke physiologically significant inotropic effects in arterioles in vivo. However, the results suggest that significant increases in arteriolar wall-to-lumen ratio occur in the earliest stages (3 days) of hypertension and probably contribute to the elevated resistance.


2015 ◽  
Vol 24 (01) ◽  
pp. 7-10 ◽  
Author(s):  
M. Pfeifer ◽  
M. Sinaki

SummaryThe objective of exercise in the treatment of osteoporosis is to improve axial stability through strengthening of back extensor muscles. Therefore, a back extension exercise program specific to one’s musculoskeletal competence and pain can be performed in a sitting position and later advanced to the prone position. When fragility is resolved, back extension is performed against resistance applied to the upper back. A significant reduction in back pain, kyphosis, and risk of falls and an improvement in the level of physical activity have been achieved through the SPEED (Spinal Proprioceptive Extension Exercise Dynamic) program. In addition, the application of a “Posture Training Support” (PTS) using a backpack may decrease kyphosis and pain related not only to compression fractures but also reduce iliocostal friction. Therapeutic exercise should address osteo - porosis-related deformities of axial posture, which can increase risk of fall and fracture. Thus, the role of a therapeutic exercise program is to increase muscle strength safely, decrease immobility-related complications, and prevent fall and fracture. As with pharmacotherapy, therapeutic exercises are individualized.


1991 ◽  
Vol 65 (02) ◽  
pp. 160-164 ◽  
Author(s):  
Marina Poggio ◽  
Armando Tripodi ◽  
Guglielmo Mariani ◽  
Pier Mannuccio Mannucci ◽  

SummaryBeing a putative predictor of ischemic heart disease, the measurement of factor VII (FVTI) coagulant activity will be presumably requested to clinical laboratories with increasing frequency. To assess the influence on FVII assays of different thromboplastins and FVII-deficient plasmas we compared performances of all possible combinations of 5 thromboplastins and 6 deficient plasmas. The reproducibility of the clotting times of the dose-response curves for human and rabbit thromboplastins were acceptable (CV lower than 7%), whereas bovine thromboplastin had a higher CV. Reproducibility was very similar for all deficient plasmas when they were used in combination with a given thromboplastin. Responsiveness of the dose-response curve did not depend on the deficient plasma but rather on the thromboplastin: one rabbit thromboplastin was the least responsive, the bovine thromboplastin the most responsive, the human and the remaining two rabbit thromboplastins had intermediate responsiveness. Assay sensitivity to cold-activated FVII varied according to the thromboplastin: the bovine thromboplastin was the most sensitive, the human thromboplastin the least sensitive, of the three rabbit thromboplastins two were relatively sensitive, one was almost insensitive. In conclusion, our results indicate that thromboplastin rather than deficient plasma is the crucial factor in the standardization of FVII assay.


1967 ◽  
Vol 56 (4) ◽  
pp. 619-625 ◽  
Author(s):  
Hans Jacob Koed ◽  
Christian Hamburger

ABSTRACT Comparison of the dose-response curves for LH of ovine origin (NIH-LH-S8) and of human origin (IRP-HMG-2) using the OAAD test showed a small, though statistically significant difference, the dose-response curve for LH of human origin being a little flatter. Two standard curves for ovine LH obtained with 14 months' interval, were parallel but at different levels of ovarian ascorbic acid. When the mean ascorbic acid depletions were calculated as percentages of the control levels, the two curves for NIH-LH-S8 were identical. The use of standards of human origin in the OAAD test for LH activity of human preparations is recommended.


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